Mutational Cooperativity Linked to Combinatorial Epigenetic Gain of Function in Acute Myeloid Leukemia
Open accessAbstract
Specific combinations of acute myeloid leukemia (AML) disease alleles, including FLT3 and TET2 mutations, confer distinct biologic features and adverse outcome. We generated mice with mutations in Tet2 and Flt3, which resulted in fully penetrant, lethal AML. Multipotent Tet2(-/-);Flt3(ITD) progenitors (LSK CD48(+)CD150(-)) propagate disease in secondary recipients and were refractory to standard AML chemotherapy and FLT3-targeted therapy. Flt3(ITD) mutations and Tet2 loss cooperatively remodeled DNA methylation and gene expression to an extent not seen with either mutant allele alone, including at the Gata2 locus. Re-expression of Gata2 induced differentiation in AML stem cells and attenuated leukemogenesis. TET2 and FLT3 mutations cooperatively induce AML, with a defined leukemia stem cell population characterized by site-specific changes in DNA methylation and gene expression.
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Combined loss of Tet2 and Dnmt3A or presence of AML-associated gene lesions impairing myeloid cell maturation triggers malignant transformation of Tet2-deficient mouse HSC.
“Only combined loss of Tet2 and Dnmt3A (18) or presence of AML-associated gene lesions impairing myeloid cell maturation triggers malignant transformation of Tet2-deficient mouse HSC (13).”
From PU.1-Dependent Enhancer Inhibition Separates <i>Tet2</i> -Deficient Hematopoiesis from Malignant Transformation (2022) · cites this paper as [13]
The Results sections on Tet2 loss with Flt3ITD report AML in double-mutant mice, altered differentiation, and leukemia-initiating activity in LSK cells. The paper identifies the self-renewing leukemia-initiating population more specifically as multipotent progenitors, not long-term HSCs, and tests Flt3ITD rather than AML-associated lesions generally. The separate Tet2–Dnmt3A clause is attached to a different citation. (LLM, conf=0.82)
Experimental — accuracy not yet measuredUREHET, Tet2HET and Tet2KO single mutant mice develop a late-onset myeloproliferative phenotype.
“both of the latter develop a late-onset myeloproliferative phenotype (Supplementary Fig. S2B–S2I; refs. 13, 17).”
From PU.1-Dependent Enhancer Inhibition Separates <i>Tet2</i> -Deficient Hematopoiesis from Malignant Transformation (2022) · cites this paper as [13]
The Results section (page unavailable) reports that some Tet2 knockout mice died after more than a year from progressive myeloproliferative neoplasms, supporting a late-onset phenotype in that single-mutant group. The Introduction also says Tet2 mutant mice develop chronic myeloproliferative disease, but the copy does not establish this phenotype specifically for Tet2HET single mutants or address UREHET mice. (LLM, conf=0.84)
Experimental — accuracy not yet measuredMPPGM appears to be a nexus of myeloid expansion under both inflammatory conditions and in animal models of myeloid malignancy.
“It is noteworthy that MPPGM (also commonly referred to as MPP3) (Challen et al., 2021) appears to be a nexus of myeloid expansion under both inflammatory conditions and in animal models of myeloid malignancy (Schepers et al., 2013; Pietras et al., 2015; Shih et al., 2015; Pietras et al., 2016; Herault et al., 2017; Hernandez et al., 2020; Kang et al., 2020; Rabe et al., 2020).”
From PU.1 is required to restrain myelopoiesis during chronic inflammatory stress (2023) · cites this paper as Shih et al., 2015
The Results section reports selective expansion of MPPs in a Tet2/Flt3ITD mouse model of AML and shows that sorted MPPs can propagate leukemia after transplantation. It does not identify those cells specifically as MPPGM/MPP3 or examine their role under inflammatory conditions. (LLM, conf=0.86)
Experimental — accuracy not yet measured
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- Authors
- Shih, A. H., Jiang, Y., Meydan, C., Shank, K., Pandey, S., Barreyro, L., Antony-Debre, I., Viale, A., Socci, N., Sun, Y., Robertson, A., Cavatore, M., de Stanchina, E., Hricik, T., Rapaport, F., Woods, B., Wei, C., Hatlen, M., Baljevic, M., Nimer, S. D., Tallman, M., Paietta, E., Cimmino, L., Aifantis, I., Steidl, U., Mason, C., Melnick, A., & Levine, R. L.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Weill Cornell Medicine (US)
- Albert Einstein College of Medicine (US)
- University of Miami (US)
- Montefiore Medical Center (US)
- Howard Hughes Medical Institute (US)
- Cornell University (US)
- Corresponding author
- Melnick, Ari
- Levine, Ross L.
- ORCID
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2015-04
- Volume
- 27
- Issue
- 4
- Pages
- 502-515
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC4518555
- OpenAlex
- W1977440531
- Cited by
- 236
- References
- 50
- Citations by year
- 2026: 12 · 2025: 15 · 2024: 12 · 2023: 15 · 2022: 18 · 2021: 22 · 2020: 25 · 2019: 23 · 2018: 19 · 2017: 33 · 2016: 31 · 2015: 11
- FWCI
- 22.62
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- National Human Genome Research Institute (R01HG006798)
- National Cancer Institute (U10CA180820, R01CA166429, CA172636-01, R01CA169784, R01CA173636, U10CA180827, U10CA021115, P30CA008748, P30CA013330, U24CA196172, R01CA166835)
- National Institute of Neurological Disorders and Stroke (R01NS076465)
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- acute myeloid leukemia, TET2, FLT3-ITD, DNA methylation, GATA2, leukemia stem cells, leukemogenesis, mouse model, chemoresistance
- MeSH terms
- Antineoplastic Agents, Cell Differentiation, Cytarabine, DNA-Binding Proteins, Doxorubicin, Mutation, Proto-Oncogene Proteins, Leukemia, Myeloid, Acute, Gene Expression Regulation, Neoplastic, DNA Methylation, Gene Silencing, Epigenesis, Genetic, Dioxygenases, GATA2 Transcription Factor, fms-Like Tyrosine Kinase 3, Haploinsufficiency
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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